Dynamics of pathological changes in brain tissue following cardiac arrest induced ischemia related to the findings of double tracer autoradiography of 45Ca and [3H] leucine uptake as respective indicators of ischemic injury and metabolic disturbance. Abnormal calcium accumulation, determined by 45Ca uptake, was related to injured but still living neurons and to reactive glial elements. 45Ca autoradiography confirmed a high sensitivity to neuronal injury of the nucleus reticularis thalami (NRT), hippocampal CA1 pyramidal layer, inferior colliculus, ventral thalamic nucleus (VTN), caudate nucleus and parietal cortex. [3H]leucine incorporation revealed that an initially widespread inhibition of protein synthesis was followed by its considerable recovery. Observations concerning the hippocampal CA1 sector and VTN suggested that a significant degree of protein synthesis, maintained at the late stage after postischemic recovery, was related to survival and regeneration of neurons and not to the presence of glial elements.